Semaglutide nafld data Just published but maybe old.
https://onlinelibrary.wiley.com/doi/full/10.1111/apt.16608
Given it's in NAFLD rather than NASH patients it seems to have some similarities to the Tesamorelin data in its ability to reduce liver fat and just slow fibrosis. Some interesting arguments why that might be we could apply to tesamorelin.
It's easy to think thtx don't have the most complete of data sets but at the same time think they are playing in the same ballpark as some of the leading drugs. I guess my hope is that if NovoNordisk took a look at tesamorelin they would recognize similarities to their own leading drug candidate.
From the discussion
"Although more subjects receiving semaglutide compared with placebo achieved a ≥ 15% reduction in liver stiffness assessed by MRE, this difference was not significant. One possible reason why a significant difference was not observed is that MRE is not sufficiently sensitive to detect changes in fibrosis in patients with less advanced disease.10, 27 A limitation of our trial is that few subjects (15% overall) had advanced disease/a high degree of liver stiffness (≥3.64 kPa) at baseline, which may have made it difficult to detect a decrease in liver stiffness. The average MRE of 2.95-3.08 kPa for the trial population at baseline corresponds to a borderline histological fibrosis of stage 1-2, while the baseline PDFF values correspond to grade 2-3 steatosis.32 Another possible reason for the lack of significant reduction in liver stiffness in our trial is the timepoint of 48 weeks. Although 48 weeks was sufficient to show NASH resolution with liraglutide in a previous study,18 in a recent study21 semaglutide showed no improvement in liver stiffness after 72 weeks; this may indicate that a much longer timeframe is required to detect an improvement in liver stiffness. Consistent with the liver stiffness findings recorded via MRE, VCTE assessment showed no significant differences between semaglutide and placebo.
Given that hepatic lipotoxicity is a prominent driving force of fibrosis progression and that steatosis and NASH are both reversible conditions,29, 33 our results showing that semaglutide reduces fat content in hepatocytes suggest the potential to reverse steatosis and halt fibrosis progression. Indeed, fewer subjects treated with semaglutide had a ≥ 15% increase in liver stiffness (MRE) compared with placebo at weeks 48 and 72. A 15% increase in liver stiffness assessed by MRE may be associated with fibrosis progression, including transition from early to advanced fibrosis."